RW Cochleostomy: A Cause of Progressive Hearing Loss?

By Thomas J. Balkany, MD



Up to one-third of recipients who retain residual hearing after CI have progressive low-frequency loss in the weeks or months after surgery.1,2

One common theory is that following CI electrode insertion, intra-scalar histiocytic and giant-cell infiltration (foreign body reaction), fibrosis and osteoneogenesis lead to the progressive loss.3,4 These inflammatory reactions may destroy residual neural elements or interfere with the fluid-pressure wave as well as basilar membrane vibration. But are intra-cochlear factors the only causes of progressive loss and does the location of the cochleostomy make a difference?

New Information

Stephen O’Leary’s lab at the University of Melbourne recently compared histological and ABR effects of RWM and bony cochleostomy in guinea pigs. The authors also observed the effects of electrode position in Scala tympani on progressive loss.5 Some of their major findings relevant to this post:

1) Bony cochleostomy did not cause progressive low-frequency hearing loss.

2) RWM incision and muscle seal (with or without electrode insertion) resulted in progressive 2 kHz hearing loss (p < 0.01). Mean threshold ABR shifts (from pre-op) at 2kHz were:

  • 1 week 6.3 (+/- 3.7) dB
  • 6 weeks 22.9 (+/- 3.4) dB

3) Intra-scalar electrode position, tissue damage and inflammatory response did not appear to be associated with progressive hearing loss.

Take Home

The cause of progressive, post-CI hearing loss may be fibrosis in the RW niche associated with the muscular tissue seal. This is consistent with a previous theory6,7 that fibrosis can reduce compliance of the RWM leading to diminished amplitude of the travelling wave, mostly in the apex (low frequency place).

If these results can be replicated and generalized, they call for further study of our techniques of sealing the RWM after electrode insertion. Are mass and/or stiffness of the RWM actually increased by incision and tissue seal; does this result in reduced amplitude of the travelling wave; how can we minimize the mass and stiffness of the RW without compromising the seal (fascia, areolar tissue, growth factors)?


    1. Woodson EA, Reiss LAJ, Turner CW, Gfeller K, Gantz BJ, 2010. The hybrid cochlear implant: a review. Adv. Otorhinolaryngol. 67, 125-134.

    2. Gstoettner W, Helbig S, Maier N, Kiefer J, Radeloff A, Adunka O. Ipsilateral electric acoustic stimulation: results of long-term hearing preservation. Audiol. Neurotol. 11(1), 49 – 56.

    3. Nadol, J.B., Eddington, D.K., Burgess, B.J., 2008. Foreign body or hypersensitivity granuloma of the inner ear after cochlear implantation: one possible cause of a soft failure? Otol. Neurotol. 29 (8), 1076-1084.,

    4. Seyyedi, M., Nadol Jr JB, 2014. Intracochlear inflammatory response to cochlear implant electrodes in humans. Otol. Neurotol. 35 (9), 1545-1551.

    5. Rowe D, Chambers S, Hampson A, Eastwood H, Campbell L, O’Leary S. Delayed low frequency hearing loss caused by cochlear implantation interventions via the round window but not cochleostomy. Hear Res 2015 333:49-57.

    6. Choi C., Oghalai J. 2005. Predicting the effect of post-implant cochlear fibrosis on residual hearing. Hear. Res.; 205: 193-200.

    7. Richards SH, 1981. Congenital absence of the round window treated by cochlear fenestration. Clin. Otolaryngol. 6 (4), 265-269.

Leave a Comment

Natasha Mcdougald 2 years ago

This a very interesting read - thanks for posting!

Loren Bartels 2 years ago

Progressive hearing loss after cochlear implant appears by assembling a variety of papers to be due to initiation of the cytokine system. What is now clear (Nadol's group) is that native cells exist in the inner ear that can become macrophages. Blood ingress include large platelets loaded with cytokines and factors that turn on macrophages. The process turns on the apoptosis cycles in various ways. The question is what measures might reduce these destructive processes. Silicone can bind to toxins: Nadol's group showed that the inflammation is predominant at the cochlesotomy and thins out but follows the carrier electrode. Would progressive hearing loss be less if the cochlesotomy seal at least on its interior surface were not tissue and did not allow blood ingress?

Chris James 2 years ago

Dear Tom, I think better definition of exactly how the RW is opened and sealed is important. Pure RW appears currently to be the most successful approach for HP - however some call extended RW "RW" etc. Why do "extended RW"? - it seems to be theoretically ideal for array trajectory but traumatises both the RW and the bone - worst of both worlds? We see plenty of cases with int/ant cochleostomy who have kept the hearing for years - however in RW I see only certain centres being successful in long term HP. Chris